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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #193735
Title: LONG-TERM VITAMIN E SUPPLEMENTATION REDUCES ATHEROSCLEROSIS AND MORTALITY IN LDLR-/-MICE

Author
item BAND, MICHAEL - TUFTS/HNRCA
item GOUTIS, JASON - TUFTS/HNRCA
item Ordovas, Jose
item Meydani, Mohsen

Submitted to: FASEB Letters
Publication Type: Abstract Only
Publication Acceptance Date: 11/15/2005
Publication Date: 4/2/2006
Citation: Band, M., Goutis, J., Ordovas, J., Meydani, M. 2006. Long-term vitamin e supplementation reduces atherosclerosis and mortality in ldlr-/-mice. FASEB Letters. 20:A1316.

Interpretive Summary:

Technical Abstract: Epidemiological and experimental evidence indicated potential health benefits of vitamin E supplementation (+E) on coronary heart disease (CHD), but recent clinical trials reported no effect. We hypothesized that +E from early age may prevent or retard development and progression of atherosclerosis and CHD mortality. To test this hypothesis, 250 LDLR-/- mice were divided into groups receiving high fat/chol diet (HFHC), moderate fat/chol (MFMC), or low fat/chol (LFLC) diets. The HFHC and MFMC groups were further subdivided into groups (N=25) receiving respective diets with +E (500 IU E/kg diet) for 0, 6, 12 and 18 mo. The diet of LFLC groups contained either +E or not (N=25). After 18 mo, plasma cholesterol was high in all dietary groups and plasma E was high in +E groups. Body weight was highest in HFHC groups and lowest in LFLC groups. Higher mortality was observed among mice treated with HFHC (48 %) and MFMC (49 %) than LFLC group (22 %). +E diets had no significant effect on mortality and extent of aortic lesions in HFHC or LFLC mice regardless of supplementation time and duration. However, mortality was significantly (p=0.04) lower among the LFLC mice receiving +E diet from early life than those that did not receive +E diet (2 vs. 9). This observation coincided with a lesser extent of aortic lesions in +E compared to LFLC mice without +E (50 vs. 65%, p=003). In conclusion, a relatively low dose and long-term E supplementation is effective in reducing mortality and atherosclerotic lesions when the diet of genetically prone mice contains low fat and low cholesterol.